Context
High affinity autoantibodies specific for the Fc regions of IgG are known as rheumatoid factors (RFs) and occur in the major of adults with rheumatoid arthritis (RA). The mechanisms behind the survival of these autoantibodies are not known, as it would be expected that cross-linking of Ig on the surface of a B cell would lead to anergy of deletion. Previous studies have, however, suggested that T cell help, delivered around the time of surface Ig cross-linking on B cells, leads to activation and secretion of higher affinity RFs. To identify the factor(s) required for the survival and differentiation of murine B cells transgenic for pathogenic high affinity human RF.